The objective of the study was to assess the relationship between breastfeeding and lower respiratory tract infections (LRTIs) during the first year of life, with special reference to maternal smoking. A cohort of 3,754 children born in 1992-1993 in the City of Oslo, Norway was recruited and data were collected at birth, 6 and 12 months of age. Complete information was obtained from 3,238 children (follow-up rate 86%). The main outcome was an episode of a LRTI, such as pneumonia, bronchitis or bronchiolitis, based on a self-administered questionnaire addressed to parents when the child was 6 and 12 months old. The outcome was specified as physician-diagnosed. In logistic regression analysis adjusting for confounding, maternal smoking increased the risk of LRTIs in children breastfed for 0-6 months (odds ratio (AOR) 1.7; 95% confidence interval (95% CI) 1.2-2.4), but not essentially when the child was breastfed for more than 6 months (AOR 1.1; 95% CI 0.7-1.6). Short-term breastfeeding (0-6 months) and no maternal smoking was related to an adjusted AOR of LRTIs of 1.3 (95% CI 1.0-1.7), and short-term breastfeeding combined with maternal smoking was related to an adjusted AOR of 2.2 (95% CI 1.6-3.1), as compared with long-term breastfeeding and no maternal smoking. The present study indicates a protective effect of long-term breastfeeding on the risk of lower respiratory tract infection during the first year of life. The results suggest that the protective effect is strongest in children exposed to environmental tobacco smoke.
Chlorination of water rich in organic material is known to produce a complex mixture of organochlorine compounds, including mutagenic and carcinogenic substances. A historical cohort study of 621,431 persons living in 56 towns in Finland was conducted in order to assess the relation between historical exposure to drinking water mutagenicity and cancer. Exposure to quantity of mutagenicity was calculated on the basis of historical information of raw water quality and water treatment practices using an empirical equation relating mutagenicity and raw water pH, KMnO4 value and chlorine dose. Cancer cases were derived from the population-based Finnish Cancer Registry and follow-up time in the study started in 1970. Age, gender, time period, social class, and urban residence were taken into account in Poisson regression analysis of the observed numbers of cases using expected numbers of cases standardized for age and gender as a basis. Excess risks were calculated using a continuous variable for mutagenicity for 3,000 net rev/l exposure representing an average exposure in a town using chlorinated surface water. After adjustment for confounding, a statistically significant excess risk was observed for women in cancers of the bladder (relative risk [RR] = 1.48, 95 percent confidence interval [CI] = 1.01-2.18), rectum (RR = 1.38, CI = 1.03-1.85), esophagus (RR = 1.90, CI = 1.02-3.52), and breast (RR = 1.11, CI = 1.01-1.22). These results support the magnitude of excess risks for rectal and bladder cancers found in earlier epidemiologic studies on chlorination by-products and give additional information on exposure-response concerning the mutagenic compounds. Nevertheless, due to the public health importance of water chlorination, uncertainty related to the magnitude of observed risks, and the fact that excess risks were observed only for women, the results of the study should be interpreted with caution.
The purpose of the present study is to assess the relationship between early acute otitis media (AOM) and exposure to respiratory pathogens mediated by siblings and day-care. A prospective cohort of 3,754 Norwegian children born in 1992-93 was followed from birth through 12 months. One or more episodes of AOM had been experienced by 25% of the children before age one. Logistic regression analysis showed that siblings attending day-care is the most important risk factor for early AOM (ORadj = 1.9 (1.4-2.3)). The total number of children in the day-care setting is another determinant for early AOM (ORadj = 2.0 (1.4-2.6) in groups of 4 or more other children and ORadj = 1.3 (1.0-1.7) in groups of 1-3 other children as compared with those who are cared for alone). Siblings who attend day-care and the number of children in the child's own day-care setting are the most important determinants for AOM the first year of life.
We hypothesized that the joint effect of genetic propensity to asthma and exposure to environmental tobacco smoke on the risk of childhood asthma is greater than expected on the basis of their independent effects. We performed a population-based 4-year cohort study of 2,531 children born in Oslo, Norway. We collected information on the child's health and environmental exposures at birth and when the child was 6, 12, 18, and 24 months and 4 years of age. The outcomes of interest were bronchial obstruction during the first 2 years and asthma at the age of 4 years. Parental atopy was defined as a history of maternal or paternal asthma or hay fever. Exposure to environmental tobacco smoke was defined on the basis of questionnaire information on household smokers at birth. In logistic regression analysis adjusting for confounding, parental atopy alone increased the risk of bronchial obstruction [odds ratio 1.62; 95% confidence interval (CI) 1.10-2.40] and asthma (1.66; 95% CI, 1.08-2.54). In children without parental atopy, there was little effect of exposure to environmental tobacco smoke on bronchial obstruction (1.29; 95% CI, 0.88-1.89) and asthma (0.84; 95% CI, 0.53-1.34). The presence of parental atopy and exposure had a substantial effect both on bronchial obstruction (2.88; 95% CI, 1.91-4.32) and asthma (2.68; 95% CI, 1.70-4.22). The results are consistent with the hypothesized joint effect of parental atopy and exposure to environmental tobacco smoke. This phenomenon--denoted as effect modification of environmental exposure by genetic constitution, or gene by environment interaction--suggests that some genetic markers could indicate susceptibility to environmental factors.
BACKGROUND: It is still unclear how early-life exposure to pets is related to children's risk of developing atopy-related diseases. We estimated associations between early-life exposure to pets and atopy-related diseases at 0-4 years of life in a cohort of Norwegian children. METHODS: A population-based cohort of 2531 children born in Oslo, Norway, was followed from birth to the age of 4 years. Information on early-life exposure to pets, a number of possible confounders, and atopy-related diseases was mainly collected by questionnaire. RESULTS: In logistic regression analysis adjusting for potential confounders, the odds ratio for being exposed to pets in early life (reference category: not exposed) was, for bronchial obstruction at 0-2 years of life, 1.2 (95% confidence interval 0.9, 1.8); for asthma at the age of 4 years, 0.7 (0.5, 1.1); for allergic rhinitis at the age of 4 years, 0.6 (0.4, 1.0); and for atopic eczema at 0-6 months of life, 0.7 (0.5, 0.9). CONCLUSIONS: The results indicate that early-life exposure to pets or lifestyle factors associated with exposure to pets reduce the risk of developing atopy-related diseases in early childhood. However, these findings might also be explained by selection for keeping pets.
BACKGROUND: Events occurring during fetal life may affect the development of the immune and respiratory systems and increase the risk of asthma and allergic diseases. OBJECTIVES: We sought to elaborate the relations between the occurrence of pregnancy complications and other pregnancy-related conditions and the risk of bronchial obstruction during the first 2 years of life and the occurrence of asthma and allergic rhinitis by the age of 4 years. Pregnancy complications were considered both as predictors of the health outcomes and as possible effects caused by other prenatal factors. METHODS: A population-based, 4-year, cohort study was carried out involving 2531 children born in Oslo, Norway. We collected information on maternally related (hyperemesis, hypertension, and preeclampsia) and uterus-related complications in pregnancy (antepartum hemorrhage, preterm contractions, insufficient placenta, and restricted growth of the uterus) and the child's health and environmental exposures at birth and at 6, 12, 18, and 24 months and 4 years of age. The outcomes of interest were bronchial obstruction during the first 2 years and asthma and allergic rhinitis at the age of 4 years. RESULTS: In a logistic regression analysis adjusting for potential confounders, uterus-related, but not other pregnancy-related, complications increased the risk of bronchial obstruction (odds ratio [OR], 2.1; 95% confidence interval [CI], 1.3-3.4), asthma (OR, 3.0; 95% CI, 1.8-5.4), and allergic rhinitis (OR, 2.9; 95% CI, 1.6-5.2). These relations were similar in children of atopic and nonatopic parents. CONCLUSIONS: Uterus-related complications in pregnancy increase the risk of having asthma and allergic rhinitis in childhood.
We assessed the effect of exposure to environmental tobacco smoke on the risk of developing bronchial obstruction in a 2-year cohort study of 3,754 children born in Oslo, Norway, during a period of 15 months in 1992-1993. We collected questionnaire information on the child's health and environmental exposures at birth and when the child was age 6 months (follow up rate = 95%), 12 months (92%), 18 months (92%), and 24 months (81%). The outcome of interest was defined as two or more episodes of bronchial obstruction or one obstruction lasting more than 1 month, and it was verified by a specialist group evaluating data from questionnaires, clinical examinations, and health records. The risk of bronchial obstruction was increased in children exposed to environmental tobacco smoke (cumulative incidence = 0.109) compared with unexposed children (0.071), with an adjusted odds ratio of 1.6 [95% confidence interval (CI) = 1.3-2.1]. The effect was seen for maternal smoking alone (odds ratio = 1.6; 95% CI = 1.0-2.6), paternal smoking alone (odds ratio = 1.5; 95% CI = 1.1-2.2), and both parents smoking (odds ratio = 1.5; 95% CI = 1.0-2.2). There was no clear exposure-response pattern. The findings indicate that exposure to environmental tobacco smoke such as is experienced in Norwegian housing increases the risk of developing bronchial obstruction during the first 2 years of life.